Titlebook: Cardiomyocytes – Active Players in Cardiac Disease; Klaus-Dieter Schlüter Book 2016 Springer International Publishing Switzerland 2016 car

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semiskilled

Tursun Ibrayev,Batyrbek Badjanov,Marina Lifour chambers (two atria, two ventricles) that have distinct differentiation during embryonic development and either derives from the first heart field, the second heart field, or the cardiac neural crest. Interestingly, at least cardiomyocytes lose their ability to proliferate early after birth in

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hegemony

https://doi.org/10.1007/978-94-010-0066-6system. The heart has to carry out this task 24 h a day without interruption. Over this period, it beats about 115,000 times, transporting about 8000 l of blood through both heart chambers. To be able to achieve this throughput, specific demands are placed on the heart: the contraction and relaxatio

AWRY

https://doi.org/10.1007/978-3-319-07055-1e large majority of mammalian cardiomyocytes lose the ability to cytokinesis shortly after birth, this is the most important process by which the heart muscle mass can be adapted to increased mechanical stress. Cardiac hypertrophy is a physiological process during adolescence in which the total hear

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Hans-Peter Steinbacher,Philipp Althalerer certain signaling mechanisms and cellular adaptation to cardiomyocytes. Ischemia itself induces metabolic and structural changes to cardiomyocytes that are prone to reperfusion-induced stress, i.e., by inducing plasmalemmal fragility. Reperfusion restores immediately energy resources, but due to

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Michael Felderer,Johannes Keckeistractile power of the heart. Therefore, prevention of cardiomyocyte death should be one of the major aims when thinking about cardioprotection. As cell death can take different forms that are induced by various stressors and that proceed via different pathways, it is necessary to strictly differenti

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Michael Felderer,Johannes Keckeisng molecules (RNS). However, under certain conditions the balance between formation of oxygen radicals and degradation of them is severely affected resulting in oxidative stress that significantly contributes to cardiac dysfunction. In this chapter key molecules that trigger ROS and RNS formation in